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Supplementary material 2 (DOCX 19 kb

Relative expression of Proglucagon mRNA (gray bar) and GLP-1 protein (black bar) in colonic mucosa of a random selection of control fed and FOS fed rats

mRNA and protein levels were normalized to Actin levels. Expression is shown as means ± SEM (n = 7). **p < 0.01, ***P < 0.001<p><b>Copyright information:</b></p><p>Taken from "Impaired barrier function by dietary fructo-oligosaccharides (FOS) in rats is accompanied by increased colonic mitochondrial gene expression"</p><p>http://www.biomedcentral.com/1471-2164/9/144</p><p>BMC Genomics 2008;9():144-144.</p><p>Published online 27 Mar 2008</p><p>PMCID:PMC2311291.</p><p></p

MOESM8 of Network-based integration of molecular and physiological data elucidates regulatory mechanisms underlying adaptation to high-fat diet

Supplementary material 8 (CYS 516 kb

Data_Sheet_4_A Constraint-Based Model Analysis of Enterocyte Mitochondrial Adaptation to Dietary Interventions of Lipid Type and Lipid Load.XLSX

<p>Computational modeling of mitochondrial adaptability and flexibility in the small intestine upon different nutritional exposures will provide insights that will help to define healthy diet interventions. Therefore, a murine enterocyte-specific mitochondrial constraint-based metabolic model (named MT_mmuENT127) was constructed and used to simulate mitochondrial behavior under different dietary conditions, representing various levels and composition of nutrients absorbed by the enterocytes in mice, primarily focusing on metabolic pathways. Our simulations predicted that increasing the fraction of marine fatty acids in the diet, or increasing the dietary lipid/carbohydrate ratio resulted in (i) an increase in mitochondrial fatty acid beta oxidation, and (ii) changes in only a limited subset of mitochondrial reactions, which appeared to be independent of gene expression regulation. Moreover, transcript levels of mitochondrial proteins suggested unaltered fusion–fission dynamics by an increased lipid/carbohydrates ratio or by increased fractions of marine fatty acids. In conclusion, our enterocytic mitochondrial constraint-based model was shown to be a suitable platform to investigate effects of dietary interventions on mitochondrial adaptation and provided novel and deeper insights in mitochondrial metabolism and regulation.</p

Data_Sheet_2_A Constraint-Based Model Analysis of Enterocyte Mitochondrial Adaptation to Dietary Interventions of Lipid Type and Lipid Load.xlsx

<p>Computational modeling of mitochondrial adaptability and flexibility in the small intestine upon different nutritional exposures will provide insights that will help to define healthy diet interventions. Therefore, a murine enterocyte-specific mitochondrial constraint-based metabolic model (named MT_mmuENT127) was constructed and used to simulate mitochondrial behavior under different dietary conditions, representing various levels and composition of nutrients absorbed by the enterocytes in mice, primarily focusing on metabolic pathways. Our simulations predicted that increasing the fraction of marine fatty acids in the diet, or increasing the dietary lipid/carbohydrate ratio resulted in (i) an increase in mitochondrial fatty acid beta oxidation, and (ii) changes in only a limited subset of mitochondrial reactions, which appeared to be independent of gene expression regulation. Moreover, transcript levels of mitochondrial proteins suggested unaltered fusion–fission dynamics by an increased lipid/carbohydrates ratio or by increased fractions of marine fatty acids. In conclusion, our enterocytic mitochondrial constraint-based model was shown to be a suitable platform to investigate effects of dietary interventions on mitochondrial adaptation and provided novel and deeper insights in mitochondrial metabolism and regulation.</p

Data_Sheet_1_A Constraint-Based Model Analysis of Enterocyte Mitochondrial Adaptation to Dietary Interventions of Lipid Type and Lipid Load.XLSX

<p>Computational modeling of mitochondrial adaptability and flexibility in the small intestine upon different nutritional exposures will provide insights that will help to define healthy diet interventions. Therefore, a murine enterocyte-specific mitochondrial constraint-based metabolic model (named MT_mmuENT127) was constructed and used to simulate mitochondrial behavior under different dietary conditions, representing various levels and composition of nutrients absorbed by the enterocytes in mice, primarily focusing on metabolic pathways. Our simulations predicted that increasing the fraction of marine fatty acids in the diet, or increasing the dietary lipid/carbohydrate ratio resulted in (i) an increase in mitochondrial fatty acid beta oxidation, and (ii) changes in only a limited subset of mitochondrial reactions, which appeared to be independent of gene expression regulation. Moreover, transcript levels of mitochondrial proteins suggested unaltered fusion–fission dynamics by an increased lipid/carbohydrates ratio or by increased fractions of marine fatty acids. In conclusion, our enterocytic mitochondrial constraint-based model was shown to be a suitable platform to investigate effects of dietary interventions on mitochondrial adaptation and provided novel and deeper insights in mitochondrial metabolism and regulation.</p

Data_Sheet_3_A Constraint-Based Model Analysis of Enterocyte Mitochondrial Adaptation to Dietary Interventions of Lipid Type and Lipid Load.XLSX

<p>Computational modeling of mitochondrial adaptability and flexibility in the small intestine upon different nutritional exposures will provide insights that will help to define healthy diet interventions. Therefore, a murine enterocyte-specific mitochondrial constraint-based metabolic model (named MT_mmuENT127) was constructed and used to simulate mitochondrial behavior under different dietary conditions, representing various levels and composition of nutrients absorbed by the enterocytes in mice, primarily focusing on metabolic pathways. Our simulations predicted that increasing the fraction of marine fatty acids in the diet, or increasing the dietary lipid/carbohydrate ratio resulted in (i) an increase in mitochondrial fatty acid beta oxidation, and (ii) changes in only a limited subset of mitochondrial reactions, which appeared to be independent of gene expression regulation. Moreover, transcript levels of mitochondrial proteins suggested unaltered fusion–fission dynamics by an increased lipid/carbohydrates ratio or by increased fractions of marine fatty acids. In conclusion, our enterocytic mitochondrial constraint-based model was shown to be a suitable platform to investigate effects of dietary interventions on mitochondrial adaptation and provided novel and deeper insights in mitochondrial metabolism and regulation.</p

Comparative analysis of the presence of AMH in the female ovary.

<p>Comparative analysis of the presence of AMH in the female ovary.</p

Presence of anti-Müllerian hormone (AMH) during follicular development in the porcine ovary - Fig 1

<p>Representative AMH staining (brown) in the porcine ovary: (A) 1. Small preantral follicle, 2. Primary follicle, 3. Recruited primordial follicle, 4. Quiescent primordial follicle in which AMH staining is absent; (B) Large preantral follicle; (C) Small antral follicle. Oocytes are indicated by arrows, AMH positive granulosa cells by asterisks and theca cells by arrowheads. Scale bars represent 15 μm (A), 30 μm (B), 60 μm (C).</p

Presence of anti-Müllerian hormone (AMH) during follicular development in the porcine ovary

<div><p>Background</p><p>Anti-Müllerian hormone (AMH) is expressed by granulosa cells of developing follicles and plays an inhibiting role in the cyclic process of follicular recruitment by determining follicle-stimulating hormone threshold levels. Knowledge of AMH expression in the porcine ovary is important to understand the reproductive efficiency in female pigs.</p><p>Research aim</p><p>In the present study we investigated the expression of AMH during follicular development in prepubertal and adult female pigs by immunohistochemistry, laser capture micro-dissection and RT-qPCR.</p><p>Results and conclusion</p><p>Although in many aspects the immunohistochemical localization of AMH in the porcine ovary does not differ from other species, there are also some striking differences. As in most species, AMH appears for the first time during porcine follicular development in the fusiform granulosa cells of recruited primordial follicles and continues to be present in granulosa cells up to the antral stage. By the time follicles reach the pre-ovulatory stage, AMH staining intensity increases significantly, and both protein and gene expression is not restricted to granulosa cells; theca cells now also express AMH. AMH continues to be expressed after ovulation in the luteal cells of the corpus luteum, a phenomenon unique to the porcine ovary. The physiological function of AMH in the corpus luteum is at present not clear. One can speculate that it may contribute to the regulation of the cyclic recruitment of small antral follicles. By avoiding premature exhaustion of the ovarian follicular reserve, AMH may contribute to optimization of reproductive performance in female pigs.</p></div